&lt;p&gt;Long Non-Coding RNA NLIPMT as a Tumor Suppressor and Inhibitor of Cell Proliferation and Metastasis in Papillary Thyroid Carcinoma&lt;/p&gt;

Zhang, Fen; Cai, Yangjun; Diao, Biyu; Song, Dandan; Miao, Rongrong; Zhang, Baodan; Hu, Yingying; Zeng, Hanqian; Hu, Xiaoqu

doi:10.2147/cmar.s266807

Cited by 3 publications

(2 citation statements)

References 42 publications

Supporting

Mentioning

Contrasting

Order By: Relevance

“…The percentage of positive cells was graded as: 1 (0-25%), 2 (26-50%), 3 (51-75%), or 4 (76-100%). The expression of SNRPC were defined according to the final one obtained from the grade of intensity multiplied by the score of the percentage of positive cells: low SNRPC expression (0-5) and high SNRPC expression (6)(7)(8)(9)(10)(11)(12). clinicopathological features.…”

Section: Immunohistochemistry (Ihc)mentioning

confidence: 99%

See 1 more Smart Citation

SNRPC promotes hepatocellular carcinoma cell motility by inducing epithelial‐mesenchymal transition

et al. 2021

View full text Add to dashboard Cite

The therapeutic outcome of hepatocellular carcinoma (HCC) remains unsatisfactory because of poor response and acquired drug resistance. To better elucidate the molecular mechanisms of HCC, here we used three Gene Expression Omnibus datasets to identify potential oncogenes, and thereby identified small nuclear ribonucleoprotein polypeptide C (SNRPC). We report that SNRPC is highly up‐regulated in HCC tissues as determined using immunohistochemistry assays of samples from a cohort of 224 patients with HCC, and overexpression of SNRPC was correlated with multiple tumors, advanced stage, and poor outcome. Kaplan–Meier analysis confirmed that patients with high SNRPC expression exhibited shorter survival in four independent HCC cohorts (all P < 0.05). Furthermore, SNRPC mutations are significantly more frequent in HCC tissues than in normal liver tissues and are an early event in the development of HCC. Functional network analysis suggested that SNRPC is linked to the regulation of ribosome, spliceosome, and proteasome signaling. Subsequently, gain‐ and loss‐of‐function assays showed that SNRPC promotes the motility and epithelial–mesenchymal transition of HCC cells in vitro. SNRPC expression was negatively correlated with the infiltration of CD4+ T cells, macrophage cells, and neutrophil cells (all P < 0.05), as determined by analyzing the TIMER (Tumor IMmune Estimation Resource) database. In conclusion, our findings suggest that SNRPC has a potential role in epithelial–mesenchymal transition and motility in HCC.

show abstract

Section: Immunohistochemistry (Ihc)mentioning

confidence: 99%

“…Recently, high throughput assays and bioinformatic tools have been widely used to screen for novel differentially expressed genes (DEGs) involved in cancers [7,8]. However, results based only on single microarray data have the limitation of a high false-positive rate.…”

Section: Introductionmentioning

confidence: 99%

SNRPC promotes hepatocellular carcinoma cell motility by inducing epithelial‐mesenchymal transition

et al. 2021

View full text Add to dashboard Cite

show abstract

Epigenetic regulation of papillary thyroid carcinoma by long non-coding RNAs

Lin

Yang

Jia

et al. 2022

Seminars in Cancer Biology

View full text Add to dashboard Cite

LncRNA AL133415.1 promotes neuronal apoptosis and its association with Alzheimer's disease through the regulation of miR-125b/vimentin axis

Cheng

Zou

et al. 2023

Preprint

View full text Add to dashboard Cite

Background Accumulating studies have identified that long noncoding RNA (lncRNA) are novel regulators in Alzheimer’s disease (AD). The goal of this study is to examine the impact of LncRNAAL133415.1 on cell viability, neuronal apoptosis, and oxidative stress and to further investigate the molecular mechanisms in AD. Methods In our study, we transfected control overexpression, lncRNA AL133415.1 overexpression, control siRNA, and lncRNA AL133415.1 siRNA into an SH-SY5Y-based AD cell model that was established using Aβ42 insult. We then measured cell viability and apoptosis using a CCK-8 assay and apoptosis marker expressions. Oxidative stress was assessed using a reactive oxygen species assay Kit and RT-qPCR was used to make observations. Total proteins were extracted and quantified using Western blot assays. We also determined the expression of Vimentin in each group. Results Transcriptome analysis revealed that vimentin (VIM) is a cis-target gene regulated by lncRNA AL133415.1. TargetScan database showed that VIM is a promising candidate target gene for miR-138-5p. In AD cell model, overexpression of lncRNA AL133415.1 inhibited cell viability and promoted cell apoptosis, while silencing lncRNA AL133415.1 had the opposite effect. Similarly, overexpression of lncRNA AL133415.1 inhibited Vimentin expression, while silencing lncRNA AL133415.1 promoted Vimentin expression. Overexpression of miR-138-5p also inhibited Vimentin expression, while inhibition of miR-138-5p expression promoted Vimentin expression. The levels of ROS were reduced in the lncRNA AL133415.1 silence group and increased in the lncRNA AL133415.1 overexpression group. Conversely, SOD levels were increased in the lncRNA AL133415.1 silence group and decreased in the lncRNA AL133415.1 overexpression group. Conclusion LncRNA AL133415.1 may interact with miR-138-5p to increase neuron cell death and reduce the expression of Vimentin in AD.

show abstract

<p>Long Non-Coding RNA NLIPMT as a Tumor Suppressor and Inhibitor of Cell Proliferation and Metastasis in Papillary Thyroid Carcinoma</p>

Cited by 3 publications

References 42 publications

SNRPC promotes hepatocellular carcinoma cell motility by inducing epithelial‐mesenchymal transition

SNRPC promotes hepatocellular carcinoma cell motility by inducing epithelial‐mesenchymal transition

Epigenetic regulation of papillary thyroid carcinoma by long non-coding RNAs

LncRNA AL133415.1 promotes neuronal apoptosis and its association with Alzheimer's disease through the regulation of miR-125b/vimentin axis

Contact Info

Product

Resources

About